This investigation is concerned with the pathogenesis and pathology of encephalomyocarditis virus infections in experimental animals. This virus produces several unique lesions which serve as models of human disease. Our work is directed to elucidating the nature of these lesions and the reasons why they occur. The "M" variant of the encephalomyocarditis virus possesses the unique capacity to attack the islets of Langerhans of mice and primates, and causes a diabetes mellitus-like disease in the animal. We have investigated this condition in detail from the biochemical and morphologic viewpoints, and currently we are exploring the effects of metabolic and genetic factors on its occurrence. Work supported by this grant in the future will be concerned with elucidating the means by which EMC virus damages the beta cells of the islets of Langerhans. The encephalomyocarditis virus also attacks the myocardium of several different species of animals. The resulting lesion serves as a model of disease occurring in man. We are attempting to define the features of the cardiac lesion and the mechanisms by which the heart is damaged.